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TL-2 attenuates β-amyloid induced neuronal apoptosis through the AKT/GSK-3β/β-catenin pathway
| Content Provider | Scilit |
|---|---|
| Author | Zhu, Xiaolei Wang, Sulei Yu, Linjie Yang, Hui Tan, Renxiang Yin, Kailin Jin, Jiali Zhao, Hui Guan, Dening Xu, Yun |
| Copyright Year | 2014 |
| Description | β -amyloid (A β )-mediated neuronal apoptosis contributes to the progression of Alzheimer's disease (AD), although the exact mechanism remains unclear. This study aimed to investigate whether Dalesconol B (TL-2), a potent immunosuppressive agent with an unusual carbon skeleton, could inhibit A β -induced apoptosis in vitro and in vivo and to explore the underlying mechanisms. A $β_{1–42}$ was injected to bilateral hippocampus of mice to make the AD models in vivo . TL-2 was able to cross the blood-brain barrier and attenuate memory deficits in the AD mice. TL-2 also inhibited A $β_{1–42}$ -induced neuronal apoptosis in vitro and in vivo . In addition, TL-2 could activate the AKT/GSK-3 β pathway, and inhibition of AKT and activation of GSK-3 β partially eliminated the neuroprotective effects of TL-2. Furthermore, TL-2 induced the nuclear translocation of β -catenin and enhanced its transcriptional activity through the AKT/GSK-3 β pathway to promote neuronal survival. These results suggest that TL-2 might be a potential drug for AD treatment. |
| Related Links | https://academic.oup.com/ijnp/article-pdf/17/9/1511/6955418/17-9-1511.pdf |
| Ending Page | 1519 |
| Page Count | 9 |
| Starting Page | 1511 |
| DOI | 10.1017/s1461145714000315 |
| Journal | International Journal of Neuropsychopharmacology |
| Issue Number | 09 |
| Volume Number | 17 |
| Language | English |
| Publisher | Cambridge University Press (CUP) |
| Publisher Date | 2014-09-01 |
| Access Restriction | Open |
| Subject Keyword | International Journal of Neuropsychopharmacology Biochemistry and Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
